Abstract
Schizophrenia is a severe disorder characterized by positive, negative and cognitive symptoms, which are still not fully understood. The development of efficient antipsychotics requires animal models of a strong validity, therefore the aims of the article were to summarize the construct, face and predictive validity of schizophrenia models based on rodents and zebrafish, to compare the advantages and disadvantages of these models, and to propose future directions in schizophrenia modeling and indicate when it is reasonable to combine these models. The advantages of rodent models stem primarily from the high homology between rodent and human physiology, neurochemistry, brain morphology and circuitry. The advantages of zebrafish models stem in the high fecundity, fast development and transparency of the embryo. Disadvantages of both models originate in behavioral repertoires not allowing specific symptoms to be modeled, even when the models are combined. Especially modeling the verbal component of certain positive, negative and cognitive symptoms is currently impossible.
Highlights
Schizophrenia is a severe mental disorder affecting approximately 1% of the worldwide adult population and often ending fatally [1,2,3]
To summarize the construct, face and predictive validity of schizophrenia models based on rodents and zebrafish
Given the very high heritability index it is not surprising that more than a hundred altered genetic loci have been identified to be associated with psychosis and the number of revealed genetic factors still increases [22, 23]
Summary
Schizophrenia is a severe mental disorder affecting approximately 1% of the worldwide adult population and often ending fatally [1,2,3]. The pathophysiology stems from an imbalance in excitatory and inhibitory neurotransmission with consequent dysregulation of neuromodulation resulting in a set of positive, negative and cognitive symptoms [4]. The exact neurobiological mechanisms underlying schizophrenia symptoms are still not known and the knowledge gaps substantially limit the development of effective treatment, especially the cure of negative and cognitive symptoms [6]. Animal models of a high construct validity evaluating the ability of the model to reconstruct the etiopathogenesis of the disease, a high face validity reflecting the similarity of modeled symptoms with the disorder expression, and a high predictive validity evaluating the possibility to normalize elicited symptoms by antipsychotic drugs, are required [7, 8]
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